Abstract
BackgroundVestibular compensation is a homeostatic process that occurs in the central nervous system in response to peripheral vestibular dysfunction. Experimental studies in rodent models have suggested that unilateral peripheral vestibular lesions are correlated with an increase in the intrinsic excitability of central vestibular neurons. This process may be dependent on the intrinsic properties of the neurons themselves. We aimed to conduct a systematic review of the literature to survey the evidence for changes in intrinsic plasticity observed during the acute phase of vestibular compensation.MethodsWe systematically reviewed the literature regarding the electrophysiological effect of experimentally induced unilateral vestibular deafferentation (UVD) on the intrinsic membrane properties of medial vestibular nucleus neurons in animal models. We developed tools to assess the methodological quality (precision, validity and bias) of studies that met pre-determined inclusion and exclusion criteria. We extracted numerical data and performed a meta-analysis of specific quantitative data pooled from these studies.ResultsWe identified 17 studies that satisfied the inclusion criteria. There is moderate quality evidence to suggest a statistically significant increase in the intrinsic excitability of medial vestibular nucleus neurons following unilateral vestibular deafferentation. Specifically, the spontaneous discharge rate increases by 4 spikes/s on average and the sensitivity to current stimuli increases.ConclusionUsing this novel approach, we demonstrate that the methodology of systematic review and meta-analysis is a useful tool in the summation of data across experimental animal studies with similar aims.
Highlights
Vestibular compensation is a homeostatic process that occurs in the central nervous system in response to peripheral vestibular dysfunction
Vestibular dysfunction is characterised by distinct oculomotor and postural deficits that are observed in human subjects [1] and can be induced experimentally in animal models [2]
When unilateral vestibular deafferentation (UVD) is induced experimentally in animal models, the intensity of these deficits abates over days, such that they may only be revealed in certain circumstances [3]
Summary
Vestibular compensation is a homeostatic process that occurs in the central nervous system in response to peripheral vestibular dysfunction. The sensory information used by this system is derived from the paired vestibular organs, visual inputs and sensory and proprioceptive feedback from the limbs These signals are received by a complex of vestibular nuclei within the brainstem and distributed to brainstem oculomotor and spinal locomotor effector circuits. Vestibular dysfunction is characterised by distinct oculomotor and postural deficits that are observed in human subjects [1] and can be induced experimentally in animal models [2]. These deficits are static (present when there is no applied stimulus apart from gravity) or dynamic (revealed by movement). Static deficits have been shown to recover in the absence of visual and cerebellar [9] inputs, consistent with the idea that this is a purely vestibular phenomenon
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